• Acute renal failure is defined as sudden, rapid, potentially reversible deterioration of renal function.
It can be classified according to underlying cause as:
• Prerenal azotemia – stemming from decreased blood flow to kidneys
• Intrarenal acute renal failure – involving intrinsic damage to renal structures
• Postrenal obstruction – involving obstruction of urine outflow
II. Risk Factors
Prerenal azotemia – is caused by factors that interfere with renal perfusion.
• Hypovolemia (e.g. hemorrhage, shock, burns)
• Increased intravascular capacity (e.g. from sepsis, neurogenic bladder)
• Cardiac disorders (e.g. myocardial infarction, arrhythmias_
• Renal artery obstruction
• Hepatorenal syndrome
Intrarenal acute renal failure
• Acute tubular necrosis – which accounts for about 75% of all cases of acute renal failure
• Acute glomerulonephritis
• Acute pyelonephritis
• Ureteral obstruction due to calculi, strictures, trauma, or pregnancy
• Bladder obstruction (e.g. cancer, prostatic hypertrophy)
• The exact pathogenesis of acute renal failure is not always known, but it is associated with a severe reduction in the glomerular filtration rate. This may be caused by decreased renal blood flow that leads to increased renal-vascular resistance, increased hydrostatic pressure in Bowman’s capsule, or a disruption of tubular epithelium.
FOUR CLINICAL PHASES OF ACUTER RENAL FAILURE:
• The onset phase – extends from the time of the precipitating event to the beginning of the oliguric-anuric phase.
• The oliguric-anuric phase – is marked by urine output of less than 400 ml/day, volume overload, elevated blood urea nitrogen (BUN) and creatinine levels, electrolyte abnormalities, metabolic acidosis, and uremia.
• The diuretic phase – extends from the time that output becomes more than 400ml/day to the time the BUN stops rising and stabilizes in normal range. During this phase, electrolyte and acid-base problems begin to normalize.
• The convalescent phase – extends from the time the BUN stabilizes until the client returns to normal activity. The client may take up to 2 years to regain 70%to 80% of normal function.
Systemic effects of acute renal failure are widespread and may include:
• Fluid and electrolyte imbalances
• Increased susceptibility to infection
• Platelet dysfunction
• GI disturbances (e.g. anorexia, nausea, vomiting, diarrhea, or constipation, stomatitis)
• Uremic encephalopathy
IV. Assessment/Clinical Manifestations/Signs and Symptoms
• Altered urine output, may be oliguria, anuria, or rarely polyuria
• Hypertension or hypotension
• Signs of fluid overload or extracellular fluid depletion
Laboratory and diagnostic study findings
• In prerenal – values are higher than 900 mOsm/kg
• In intrarenal parenchymal failure – values are less than 250 mOsm/kg
• In postrenal obstruction – values may be normal
• BUN, serum creatinine, and potassium levels are elevated
• Blood pH, bicarbonate, hemoglobin, and hematocrit values are decreased
V. Medical Management
• Treatment objectives are to restore normal chemical balance and prevent complications until renal tissues are repaired and renal function is restored. Possible causes of damage are identified and treated.
• Fluid balance is managed based on daily weight, serial measurements of central venous pressure, serum and urine concentrations, fluid losses, blood pressure, and clinical status. Fluid excesses are treated with mannitol, furosemide to initiate dieresis and prevent or minimize subsequent renal failure.
• Blood flow is restored to the kidneys with the use of intravenous fluids, albumin or blood product transfusions.
• Dialysis (hemodialysis, hemofiltration, or peritoneal dialysis) is started to prevent complications of uremia, including hyperkalemia, pericarditis and seizures.
• Ion exchange resins (orally or by retention enema)
• Intravenous glucose and insulin or calcium glutamate as an emergency and temporary measure to treat hyperkalemia.
• Sodium bicarbonate to elevate plasma pH.
• Parenteral erythropoietin (Epogen) to treat reduced erythropoietin production and prevent anemia
• Shock and infection are treated if present
• Arterial blood gases are monitored when severe acidosis is present.
• If respiratory problems develops, ventilator measures are started.
• Phosphate-binding agents such as aluminum hydroxide to control elevate serum phosphate concentrations.
• Dietary protein is limited to about 1g/kg during oliguric phase to minimize protein breakdown and to prevent accumulation of toxic end products.
• Caloric requirements are met with high-carbohydrate feedings; parenteral nutrition
• Foods and fluids containing potassium and phosphorus are restricted; potassium intake is limited to 40 to 60 mEq/d. Sodium intake is restricted to 2 g/d.
• Blood chemistries are evaluated to determine amount of replacement sodium, potassium, and water during oliguric phase.
• After the diuretic phase, high-protein, high-calorie diet is given with gradual resumption of activities.